Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Gene expression of rat PSCs cultured on plastic, matrigel and collagen

ABSTRACT: Activated pancreatic stellate cells produce the fibrotic matrix in chronic pancreatitis and pancreatic cancer. In vitro protocols examining PSC biology have usually involved PSCs cultured on plastic, a non-physiological surface. However, PSCs cultured on physiological matrices e.g. MatrigelTM (normal basement membrane) and collagen (fibrotic pancreas), may have distinctly different behaviours compared to cells cultured on plastic. Therefore, we aimed to compare PSC gene expression after culture on plastic, MatrigelTM and collagen I.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE43496 | GEO | 2013/01/17

SECONDARY ACCESSION(S): PRJNA186664

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Gene expression of rat PSCs cultured on plastic, matrigel and collagen

Project description:Activated pancreatic stellate cells produce the fibrotic matrix in chronic pancreatitis and pancreatic cancer. In vitro protocols examining PSC biology have usually involved PSCs cultured on plastic, a non-physiological surface. However, PSCs cultured on physiological matrices e.g. MatrigelTM (normal basement membrane) and collagen (fibrotic pancreas), may have distinctly different behaviours compared to cells cultured on plastic. Therefore, we aimed to compare PSC gene expression after culture on plastic, MatrigelTM and collagen I. Total RNA from stellate cells in 10 cm Petri dishes was isolated by Qiagen RNeasy Mini Plus kit as per manufacturer’s instructions. The Agilent 2100 Bioanalyzer (Agilent Technologies Inc. Santa Clara, CA) was used for quality control of the isolated total RNA. Gene expression profiles of rat PSCs cultured on MatrigelTM, collagen I and plastic were analysed by whole rat genome microarray purchased from Affymetrix (Rat Gene 1.0 ST Array). This array was able to detect 27,342 rat genes, with approximately 26 probes on average per gene (referred to as a probe set).

2013-01-17 | E-GEOD-43496 | biostudies-arrayexpress

Separated Pancreatic stellate cells (PSCs) by functional separation using modified Matrigel invasion assay

Project description:We separated PSCs by functional separation using moidfied Matrigel invasion assay our previously reported (Fujiwara, PLoS One, 2012). In this culture system, we evaluated two primary cultures of human PSCs. PSCs in the upper chambers were incubated for 72 hours in culture with SUIT-2 pancreatic cancer cells in the lower chambers, or as controls without pancreatic cancer cells in the lower chambers, and were collected from the top and bottom sides of the upper chambers separately. The top side-derived PSCs were cells that did not migrate toward the cancer cells, and the bottom side-derived PSCs were cells that migrated toward the pancreatic cancer cells. We then performed a DNA microarray analysis using these cells. The quality of the RNA samples was evaluated using Experion™ Automated Electrophoresis Station (Bio-Rad Laboratories, Hercules, CA). We used a HumanHT-12v4 Expression BeadChip (Illumina, San Diego, CA) for these analyses. The data were analyzed using Bead Studio software version 3.2.3 (Illumina).

2014-02-25 | E-GEOD-55300 | biostudies-arrayexpress

Separated Pancreatic stellate cells (PSCs) by functional separation using modified Matrigel invasion assay

2014-02-25 | GSE55300 | GEO

Extracellular matrix targeted mRNA profiles of PKN2 KO/WT mouse pancreatic stellate cell lines (PSCs) treated with TGF-b or vehicle control

Project description:In pancreatic ductal adenocarcinoma (PDAC), differentiation of pancreatic stellate cells (PSCs) into myofibroblast-like cancer-associated fibroblasts (CAFs) promotes fibrotic, therapy-resistant tumours. Conversely, suppression of CAFs can result in aggressive metastatic tumours. Here we show that the Rho-effector kinase protein kinase N2 (PKN2) is critical for PSC myofibroblast differentiation. Loss of PKN2 was associated with reduced PSC proliferation and contractility, retention of lipid droplets and decreased a-SMA stress fibres. PKN2 loss was also associated with a myofibroblast CAF to -like inflammatory CAF switch in the PSC matrisome signature both in vitro and in vivo. In spheroid co-cultures with PDAC cells, loss of PKN2 prevented PSC invasion but, counter-intuitively, promoted invasive cancer cell outgrowth. Further, deletion of PKN2 in the pancreatic stroma induced more locally invasive, orthotopic pancreatic tumours. Finally, we demonstrated that a PKN2KO PKN2 KO matrisome signature predicts poor outcome in pancreatic and other solid human cancers. Our data indicate that suppressing PSC myofibroblast differentiation function can limit important stromal tumour suppressive mechanisms, while promoting a switch to a cancer-supporting CAF phenotype.

2021-11-22 | GSE189245 | GEO

RNA-Seq of flow-sorted Egfr WT or Egfr KO pancreatic stellate cells (PSCs) and flow-sorted pancreatic tumor organoids following co-culture.

Project description:We investigated changes in transcriptome in Egfr KO PSCs co-cultured with pancreatic tumor organoids compared to Egfr WT PSCs co-cultured with the same pancreatic tumor organoids. We also investigated the changes in transcriptome in pancreatic tumor organoids co-cultured with Egfr WT or Egfr KO PSCs.

2023-11-30 | GSE243838 | GEO

Rattus norvegicus

Project description:Gene expression of rat PSCs cultured on plastic, matrigel and collagen

| PRJNA186664 | ENA

RNA-Seq comparison of pancreatic stellate cells (PSCs) cultured with control media, TGF-beta, pancreatic tumor organoid conditioned media or pancreatic tumor organoid conditioned media in the presence of ERBBi (neratinib)

Project description:We investigated the role of ERBB signaling in PSCs cultured with TGF-beta (myCAFs) or pancreatic tumor organoid conditioned media (with or without ERBBi) compared to PSCs cultured with control media (quiescent PSCs)

2023-11-30 | GSE219180 | GEO

Proteome and secretory proteome of UCA-PSCs and WJ-MSCs

Project description:A total of 1× 107 cultured UCA-PSCs and WJ-MSCs at P4 were lysed with 300 μL of SDS lysis buffer containing protease inhibitor and 1 μM PMSF in 1.5-mL tubes. Each sample was ultrasonicated on ice for 3 min. After centrifugation twice at 2000 ×g for 10 min at 4°C, the supernatant was collected for total protein measurement and further LC-MS analysis. Cell supernatants (5 mL/106 cells) of P4 UCA-PSCs and WJ-MSCs cultured in basic DMEM without serum or antibiotics for 48 h were collected. After concentration in 3-KD ultrafiltration centrifuge tubes, the cell supernatants were frozen and resuspended in SDS solution. After centrifugation, the supernatants from UCA-PSC and WJ-MSC cultures were obtained.Secretory proteome of UCA-PSCs and WJ-MSCs was further analyzed.

2022-05-24 | PXD034036 | iProX

Vitamin d receptor-mediated stromal reprogramming suppresses pancreatitis and enhances pancreatic cancer therapy

Project description:The poor clinical outcome in pancreatic ductal adenocarcinoma (PDA) has been attributed to intrinsic resistance to chemotherapy and a growth-permissive tumor microenvironment. Quiescent pancreatic stellate cells (PSCs) are neuroendocrine, nestin-positive, lipid-accumulating cells whose homologues in the liver are the principal repository of Vitamin A esters. Upon activation, lipid droplets are lost and via transdifferentiation they become the key cell type responsible for driving the severe desmoplasia that characterizes PDA. Despite their critical role in PDA progression and chemoresistance, therapeutic strategies targeting PSCs are lacking. Here we identified the vitamin D receptor (VDR) as a master genomic regulator of PSC activation and function. In vitro we demonstrate that VDR activation reduces expression in PSCs of genes implicated in activation, inflammation, and extracellular matrix production, as well as restoring lipid droplet integrity. In vivo, the VDR ligand calcipotriol enhances the anti-tumor effects of gemcitabine by increasing intratumoral concentration 5-fold, reducing tumor volume to near baseline and lowering metastases by more than 65%. These findings implicate VDR as a master regulator of PSC activation and identify a novel therapeutic approach for the treatment of pancreatic cancer. RNA-Seq analyses was used to characterize cancer-associated changes between pre-activated (3-day culture) and activated (7-day culture) primary mouse PSCs, as well as control and PDA human PSCs. RNA-Seq was also used to assess the impact of VDR activation (DMSO vs calcipotriol) in a human PSC line (MiaPaCa-2), the mouse primary PSCs

2014-10-03 | E-GEOD-43770 | biostudies-arrayexpress

Disruption of pancreatic stellate cell myofibroblast phenotype promotes pancreatic tumour invasion.

2021-11-19 | GSE189027 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data